The efficacy and safety of hydrotherapy in patients with knee osteoarthritis: a meta-analysis of randomized controlled trials.

BACKGROUND: Currently, there is poor evidence of the effect of hydrotherapy on patients with knee osteoarthritis (OA). The authors performed a meta-analysis from randomized controlled trials to determine the efficacy and safety of a hydrotherapy program on measures of pain and knee function in individuals living with knee OA. METHODS: A literature review included PubMed, EMBASE, Cochrane Library, Science Citation Index, ScienceDirect, and Ovid. Studies evaluating the efficacy of hydrotherapy for knee OA up to August 2023 were included. The research was reported based on the preferred reporting items for systematic reviews and meta-analysis guidelines to ensure the reliability and verity of results. Statistical analysis was performed using Stata/SE version 15.0. RESULTS: A total of six randomized controlled trials were included for data extraction and meta-analysis. The present study revealed that there were significant differences between the two groups regarding the pain intensity at 1 week (WMD=-0.429; 95% CI: -0.679 to -0.179; P =0.001), 4 week (WMD=-0.308; 95% CI: -0.587 to -0.030; P =0.030) and 8 week (WMD=-0.724; 95% CI: -1.099 to -0.348, P <0.001). Furthermore, hydrotherapy was associated with improved outcome of the Western Ontario and McMaster Universities Arthritis index at 1 week (WMD=-3.314; 95% CI: -6.484 to -0.145, P =0.040), 4 week (WMD= -3.630; 95% CI: -6.893 to -0.366, P =0.029) and 8 week (WMD=-3.775; 95% CI: -7.315 to -0.235; P =0.037). No serious adverse events were observed in all patients who received hydrotherapy. CONCLUSION: Hydrotherapy is efficacious and safe for reducing pain and improving functional status in individuals with knee OA, without increasing the risk of adverse effects.

Jiangqi Pingxiao formula regulates dendritic cell apoptosis in an autophagy-dependent manner through the AMPK/mTOR pathway in a murine model of OVA-induced asthma.

ETHNOPHARMACOLOGICAL RELEVANCE: Allergic asthma is a recurring respiratory condition that typically manifests during childhood or adolescence. It is characterized by a dominant type II immune response triggered by the identification and capturing of inhaled allergens by dendritic cells (DCs). Jiangqi Pingxiao Formula (JQPXF), a prescription medicine used for the treatment of pediatric asthma, has been clinically proven to be both safe and effective. However, its mechanism of action in the treatment of asthma has not been fully been fully elucidated. Recent research suggests that several natural compounds have the potential to target dendritic cells (DCs) and alleviate ovalbumin (OVA)-induced asthma, which may also be found within JQPXF. AIM OF THE STUDY: This study aimed to elucidate the effect of JQPXF on OVA-induced asthma model and its molecular mechanism targeting DCs. MATERIALS AND METHODS: The main constituents of JQPXF were analyzed by ultra performance liquid chromatography (UPLC). An asthma model was established by OVA. Hematoxylin-eosin staining and measurement of respiratory function was used to evaluate the treatment effect of JQPXF on asthmatic mice. Cytokine (IL-5, IL-13 and IgE) concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Flow cytometry was employed to evaluate inflammatory cell infiltration (T helper 2 cells and DCs) in vivo and DC survival in vivo and vitro. Western blot and immunofluorescence were used to verify the molecular mechanisms. RESULTS: The results suggest that JQPXF can ameliorate pathological conditions and improve lung function in asthmatic mice, as well as the Th2 cells. Treatment with JQPXF significantly reduced the number of DCs and increased the number of Propidium iodide+ (PI) DCs. Furthermore, JQPXF upregulated protein levels of the pro-apoptotic factors Cleaved-caspase-3 and Bax, while downregulating the anti-apoptotic factor Bcl-2. Simultaneously, JQPXF increased autophagy levels by facilitating p62 degradation and promoting translation from LC3B I to LC3B II of DCs in vitro, as well as reducing the integrated optical density (IOD) of p62 within the CD11c-positive area in the lung. 3-Methyladenine (3-MA) was used to block autophagic flux and the apoptotic effect of JQPXF on DCs was abolished in vitro, with the number of DCs decreased by JQPXF being reversed in vivo. We further investigated the upstream key regulator of autophagy, the AMPK/mTOR pathway, and found that JQPXF increased AMPK phosphorylation while decreasing mTOR phosphorylation levels. Additionally, we employed Compound C (CC) as an AMPK inhibitor to inhibit this signaling pathway, and our findings revealed that both autophagic flux and apoptotic levels in DCs were abolished in vitro. CONCLUSIONS: In summary, we have demonstrated that JQPXF could alleviate type II inflammation in an asthmatic model by promoting the apoptosis of DCs through an autophagy-dependent mechanism, achieved by regulating the AMPK/mTOR signaling pathway.